Linkage of Faulty Major Histocompatibility Complex Class I to Autoimmune Diabetes
العنوان: | Linkage of Faulty Major Histocompatibility Complex Class I to Autoimmune Diabetes |
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المؤلفون: | Xiangping Li, Jane Guo, Yineng Fu, Joseph Avruch, George S. Eisenbarth, Herbert Y. Lin, Denise L. Faustman |
المصدر: | Science. 254:1756-1761 |
بيانات النشر: | American Association for the Advancement of Science (AAAS), 1991. |
سنة النشر: | 1991 |
مصطلحات موضوعية: | Cytotoxicity, Immunologic, T-Lymphocytes, T cell, Antigen presentation, Gene Expression, Genes, MHC Class I, Human leukocyte antigen, Biology, Lymphocyte Activation, Major histocompatibility complex, Autoimmune Diseases, Prediabetic State, Mice, Mice, Inbred NOD, MHC class I, Diseases in Twins, medicine, Animals, Humans, Lymphocytes, Antigen-presenting cell, Autoimmune disease, Mice, Inbred BALB C, Multidisciplinary, MHC Class I Protein, Flow Cytometry, medicine.disease, Mice, Inbred C57BL, Diabetes Mellitus, Type 1, medicine.anatomical_structure, Immunology, biology.protein, Spleen |
الوصف: | Pancreatic islet cells are the targets of an autoimmune response in type I diabetes. In the nonobese diabetic (NOD) mouse model of autoimmune diabetes, expression of major histocompatibility complex (MHC) class I proteins was inversely correlated with diabetes; in this mouse a mutation in the MHC class II-linked gene for the putative MHC class I peptide transporter was also present. Mice deficient in MHC class I expression because they do not produce beta 2-microglobulin also developed late onset autoimmune diabetes. In cells from humans with type I diabetes expression of MHC class I was decreased; subsets of prediabetics categorized as most likely to become hyperglycemic also had low MHC class I. T cell responses to self antigens are faulty in diabetics. In sets of genetically identical twins that are discordant for diabetes, the defect appeared to reside with the antigen presenting cell. Thus, a lack of surface MHC class I protein is associated with autoimmune diabetes; the concomitant defect in antigen presentation may impair the development of self tolerance, which could result in autoimmune disease. |
تدمد: | 1095-9203 0036-8075 |
URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::46dead270c340d8f1d71a86a857364f7 https://doi.org/10.1126/science.1763324 |
رقم الأكسشن: | edsair.doi.dedup.....46dead270c340d8f1d71a86a857364f7 |
قاعدة البيانات: | OpenAIRE |
تدمد: | 10959203 00368075 |
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